Cory Krediet

Postdoctoral Research fellow, Genetics

Bio

Bio

As a postdoctoral scholar in the Pringle lab, my research focuses on the genetic and molecular mechanisms involved in cnidarian-dinoflagellate symbiosis. Tropical corals and other cnidarian “holobionts,” including the sea anemone, Aiptasia form a mutualistic symbiosis with dinoflagellate algae (Symbiodinium) and other microbial partners (bacteria, archaea, viruses, and fungi). Our understanding of this symbiosis in terms of onset, maintenance, and breakdown is extremely limited, which allows us to ask many exciting and challenging questions. I am interested in genes that are differentially expressed during symbiosis and in response to environmental and biological stressors. I was born in Oklahoma, grew up in Chicago, and received by B.A. in Biology and German from Drew University. I completed by Ph.D. at the University of Florida, where I studied interactions between native coral-commensal bacteria and invading opportunistic pathogens. When I am not in the lab you can find me in the gym, in the pool, playing beach volleyball, or simply enjoying the California sun.

Professional Education

Doctor of Philosophy, University of Florida (2012)

Master of Science, University of Florida (2008)

Bachelor of Arts, Drew University (2006)

Stanford Advisors

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Research & Scholarship

Current Research and Scholarly Interests

My primary research interests lie in host-microbe interactions and specifically how mutualistic or commensal microbiota influence the hosts response to various abiotic and biotic stressors. These types of interactions are present in a wide array of systems ranging from humans and other vertebrates, to invertebrates and to plants. My current research focuses on a cnidarian-dinoflagellate symbiosis. Specifically, my research aims to identify differentially expressed genes in the host in response to thermal- and/or light-stress, which leads to a breakdown of the symbiosis. To do this, I am using the model sea anemone, Aiptasia pallida.

Abstract

The global decline of reef-building corals is due in part to the loss of algal symbionts, or "bleaching," during the increasingly frequent periods of high seawater temperatures [1, 2]. During bleaching, endosymbiotic dinoflagellate algae (Symbiodinium spp.) either are lost from the animal tissue or lose their photosynthetic pigments, resulting in host mortality if the Symbiodinium populations fail to recover [3]. The >1,000 studies of the causes of heat-induced bleaching have focused overwhelmingly on the consequences of damage to algal photosynthetic processes [4-6], and the prevailing model for bleaching invokes a light-dependent generation of toxic reactive oxygen species (ROS) by heat-damaged chloroplasts as the primary trigger [6-8]. However, the precise mechanisms of bleaching remain unknown, and there is evidence for involvement of multiple cellular processes [9, 10]. In this study, we asked the simple question of whether bleaching can be triggered by heat in the dark, in the absence of photosynthetically derived ROS. We used both the sea anemone model system Aiptasia [11, 12] and several species of reef-building corals to demonstrate that symbiont loss can occur rapidly during heat stress in complete darkness. Furthermore, we observed damage to the photosynthetic apparatus under these conditions in both Aiptasia endosymbionts and cultured Symbiodinium. These results do not directly contradict the view that light-stimulated ROS production is important in bleaching, but they do show that there must be another pathway leading to bleaching. Elucidation of this pathway should help to clarify bleaching mechanisms under the more usual conditions of heat stress in the light.